Patients with diastolic heart failure, hypertension and hypertrophy can exhibit elevated cardiac afterload. Cardiac afterload, the impedance to ventricular emptying by aortic pressure, can substantially determine regulation of cardiac output. Cardiac output is the volume of blood flow from the heart which is the heart rate (i.e. the rate of contraction) multiplied by the stroke volume which is the amount of blood pumped out from the heart with each contraction. A high cardiac afterload significantly reduces cardiac output whereas a reduced cardiac afterload increases cardiac output.
Current therapies rely on drugs to reduce cardiac afterload. At least two disadvantages are associated with drugs to reduce cardiac afterload. First, while drugs have had limited success, some patients are nonresponders. Second, chronic use of drugs to reduce cardiac afterload have some undesirable side affects. Therefore, it is desirable to develop therapies that overcome the disadvantages associated with drugs.